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Public school art education in the United States has been around for over 125 years. Professional art education associations of one kind or another have been with us for at least 100 years. The National Art Education Association has provided information and support to art teachers for many decades, but the truth is that most public school art teachers battle constantly for recognition, adequate funding, adequate classroom and storage space, and support--often without success. This author, a member of NAEA for 48 years, expresses his view that the overwhelming preponderance of negative attitudes about art education from people outside the profession is being ignored. He states that it is way past time to get our "heads out of the sand." The sand is much deeper these days because of increasingly diverse student and parent populations, and major repercussions from the 9/11 tragedy. These two factors are not the focus of this material but weigh heavily on art teachers and art programs. Presented in this paper are comments from two retired elementary art teachers to support this point of view. A conclusion contains insights regarding potential directions for developing positive attitudes and relationships. (Contains 2 notes.)

The development of pulmonary metastasis is the leading cause of death in osteosarcoma (OS), which is the most common malignant bone tumor in children. We have previously reported that the tumor suppressor p27 (KIP1, CDKN1B) is frequently mislocalized to the cytoplasm of OS. However, its prognostic significance and metastatic mechanism are still elusive. Here, we show that cytoplasmic p27 significantly correlated with a higher metastatic status and poorer survival of OS patients (n = 136, P < 0.05), highlighting the clinical significance of p27 mislocalization in OS. Mechanistically, cytoplasmic p27 is co‐immunoprecipitated with p21‐activated kinase 1 (PAK1), which resulted in higher PAK1 phosphorylations, actin polymerization, and cell motility in p27‐mislocalized OS cells. Silencing PAK1 expression in different p27‐mislocalized OS cell lines decreased the migratory and adhesion abilities in vitro, as well as the development of pulmonary metastases in vivo. Similar PAK1‐dependent motility was also observed in other p27‐mislocalized cancer cell lines. In summary, our study suggests that cytoplasmic p27‐mediated PAK1 activation is crucial for OS metastasis. A biomarker‐guided targeted therapeutic approach for metastatic OS and other cancers harboring p27 mislocalization can be developed, where cytoplasmic p27 is used for risk stratification and PAK1 can be exploited as a potential therapeutic target. [ABSTRACT FROM AUTHOR]

Designers spend more resources to develop better mobile experiences today than ever before. Researchers commonly use visual search efficiency as a usability measure to determine the time or effort it takes someone to perform a task. Previous research has shown that a computational visual saliency model can predict attentional deployment in stationary desktop displays. Designers can use this salience awareness to co-locate important task information with higher salience regions. Research has shown that placing targets in higher salience regions in this way improves interface efficiency. However, researchers have not tested the model in key mobile technology design dimensions such as small displays and touch screens. In two studies, we examined the influence of saliency in a mobile application interface. In the first study, we explored a saliency model's ability to predict fixations in small mobile interfaces at three different display sizes under free-viewing conditions. In the second study, we examined the influence that visual saliency had on search efficiency while participants completed a directed search for either an interface element associated with high or low salience. We recorded reaction time to touch the targeted element on the tablet. We experimentally blocked high and low saliency interactions and subjectively measured cognitive workload. We found that a saliency model predicted fixations. In the search task, participants found highly salient targets about 900 milliseconds faster than low salient targets. Interestingly, participants did not perceive a lighter cognitive workload associated with the increase in search efficiency. [ABSTRACT FROM AUTHOR]

Severe manifestations of systemic lupus erythematosus (SLE), antiphospholipid syndrome (APS), and thrombotic thrombocytopenic purpura (TTP) are characterized by multiorgan thrombotic microangiopathy. We describe reduction of ADAMTS13 activity and the development of systemic autoimmunity in all 8 children initially diagnosed with acquired noncongenital TTP during an 8.5-year period. Median age at diagnosis was 12.0 years (range, 2.6-17.3 years). ADAMTS13 activity was absent (<5%) in 6 patients; 3 patients had a detected inhibitor. SLE was diagnosed concurrently in 3 patients, and 4 patients were diagnosed within 5 years. Six of the children diagnosed with SLE had absent ADAMTS13 activity at diagnosis. In 6 patients with SLE, immune-mediated nephritis developed by 46 months. All surviving patients with SLE developed antiphospholipid antibodies, including some with a lupus anticoagulant. Patients with SLE did not have TTP recurrences once daily immunosuppressive regimens were started. An evaluation for SLE/APS is warranted in children and adolescents with reduced ADAMTS13 activity and thrombotic microangiopathy. [ABSTRACT FROM AUTHOR]

Background: In our rat model for anti-GBM GN, severe fibrosis follows glomerular inflammation. A potential role of extracellular matrix protein osteopontin (OPN) in glomerular fibrosis was investigated.Methods: Neutralizing OPN antiserum or control normal serum was injected into the experimental rats at late inflammatory/early fibrotic stage. Glomerular inflammation and fibrosis were determined.Results: OPN antiserum treatment had little effect on glomerular inflammation. However, the antiserum treatment resulted in a significant reduction in number of fibrotic glomeruli (50% of the controls). Histology observation showed that fibrotic tissue in glomeruli of the antiserum treated rats was mild and poorly developed. OPN antiserum treatment resulted in downregulated glomerular expression of collagen 1α1; collagen deposition in the antiserum treated rats reduced to <30% of that for normal serum controls.Conclusion: Neutralization of OPN inhibited progression of fibrosis in vivo when given at early fibrotic stage. Thus, OPN may be a therapeutic target for glomerular fibrosis. [ABSTRACT FROM AUTHOR]

Background: Glomerular fibrosis is the common end result of glomerulonephritis (GN) regardless of etiology. In our rat model for anti-glomerular basement membrane GN, severe fibrosis follows glomerular inflammation. We investigated the association between expression of extracellular matrix (ECM) proteins and progression of glomerular fibrosis.Methods: Expression of ECM genes in glomeruli was determined at RNA and protein levels. Immunofluorescence was applied to identify cell sources for the molecules.Results: DNA microarray for ECM genes, quantitative RT-PCR and Western blot revealed significant upregulation of osteopontin (OPN), a multifunctional molecule, in the glomeruli only after onset of glomerular fibrosis. Two-dimensional electrophoresis showed that the expressed OPN was in three major isoforms. Immunofluorescence showed that fibrotic tissues in glomeruli accumulated massive deposits of extracellular OPN. Both in vivo and in vitro experiments showed that a novel population of multinucleated α-smooth muscle actin(+)CD90(-) myofibroblast-like cells, which surrounded fibrotic tissue, was the main source of OPN during progression of fibrosis. Since senescence-associated β-galactosidase activity was detected in those cells both in vitro and in vivo, these cells probably were terminally differentiated senescent myofibroblasts.Conclusion: OPN has been implicated in fibrosis in several organs. Our results suggest potential roles of OPN and its main source, the senescent myofibroblasts, in glomerular fibrosis. [ABSTRACT FROM AUTHOR]

Abstract: Total knee arthroplasties with an asymmetric tibial tray and posterior femoral condyles were implanted in 224 knees. Follow-up averaged 6.3 years. All components were cemented, all patellae were resurfaced, and all femoral components were cruciate-substituting. Postoperative alignment averaged 3.3° valgus. Radiolucencies were absent around 116 knees (66%). No components were radiographically loose. Knee Society scores averaged 85 postoperatively and modified Western Ontario and McMaster Universities Index scores averaged 82. Postoperative flexion averaged 114°. Ten knees required manipulation for arthrofibrosis. Lateral release was necessary in 62 knees (28%). No revisions were required for aseptic loosening. Survivorship free of additional surgical procedures was 97% at 5 years. Compared with other series by designing surgeons, similar excellent survivorship was seen but with a higher lateral release rate. [Copyright &y& Elsevier]

The “Scratch Test” uses a sharp scalpel to scrape areas of suspected tendinosis in the management of lateral and medial epicondylitis. As claimed in the literature, this tissue is friable and peels off, whereas normal tendon does not. The purpose of this study was to determine whether, or not, the “Scratch Test” is able to differentiate between tendinosis and more normal adjacent tendon. Nineteen specimens from patients treated for tendinosis about the elbow were examined histologically. Three groups of specimens were compared: (1) grossly abnormal tendon, (2) tendon that was scraped out using the “Scratch Test” and (3) tendon that remained behind following the “Scratch Test”. There was no significant histological difference between visibly degenerated tendon (group 1) and that which was scraped out using the “Scratch Test” (group 2). There was, however, a significant histological difference between both these groups and the more normal tendon tissue that the “Scratch Test” left behind (group 3). [ABSTRACT FROM PUBLISHER]

The extracellular matrix of epithelial tumors undergoes structural remodeling during periods of uncontrolled growth, creating regional heterogeneity and torsional stress. How matrix integrity is maintained in the face of dynamic biophysical forces is largely undefined. Here we investigated the role of fibulin-2, a matrix glycoprotein that functions biomechanically as an inter-molecular clasp and thereby facilitates supra-molecular assembly. Fibulin-2 was abundant in the extracellular matrix of human lung adenocarcinomas and was highly expressed in tumor cell lines derived from mice that develop metastatic lung adenocarcinoma from co-expression of mutant K-ras and p53. Loss-of-function experiments in tumor cells revealed that fibulin-2 was required for tumor cells to grow and metastasize in syngeneic mice, a surprising finding given that other intra-tumoral cell types are known to secrete fibulin-2. However, tumor cells grew and metastasized equally well in Fbln2-null and -wild-type littermates, implying that malignant progression was dependent specifically upon tumor cell-derived fibulin-2, which could not be offset by other cellular sources of fibulin-2. Fibulin-2 deficiency impaired the ability of tumor cells to migrate and invade in Boyden chambers, to create a stiff extracellular matrix in mice, to cross-link secreted collagen, and to adhere to collagen. We conclude that fibulin-2 is a driver of malignant progression in lung adenocarcinoma and plays an unexpected role in collagen cross-linking and tumor cell adherence to collagen. [ABSTRACT FROM AUTHOR]

Hypoxia occurs in many tumors and reduces the effectiveness of radio- and chemotherapy. Hypoxia also impedes immune responses to tumors, reducing T lymphocyte production of cytokines such as interleukin-2 (IL-2) and interferon gamma, as well as the survival and proliferation of these cells. We constructed a lentiviral vector encoding a bidirectional hypoxia-inducible responsive element (HRE) derived from human vascular endothelial growth factor, which drives the hIL-2 gene and a marker gene. We used a model of human B cell lymphoma to show that tumor-specific T cells modified with this vector upregulate hIL-2 expression when oxygen tension is low in vitro and in vivo. The consequence of this effect is to increase T-cell survival and proliferation whilst sustaining effector function, even in O2 concentrations as low as 1%. The phenotype of the transduced cells is unchanged, as is their ability to migrate to tumor. HRE-IL-2-modified cytotoxic T lymphocytes (CTLs) produce faster and more complete tumor regression than parental CTLs and increase overall survival. Hypoxia-resistant T cells may thus be of value in the treatment of human tumors in which areas of hypoxia may otherwise account for resistance to this therapeutic strategy.Molecular Therapy (2008); 16 3, 599–606. doi:10.1038/sj.mt.6300391 [ABSTRACT FROM AUTHOR]